Preface ....................................................... xxi
Author ...................................................... xxiii
Chapter 1
Perception and Transduction of Plant Signals in Pathogens ....... 1
1.1 Introduction ................................................ 1
1.2 Signaling and Transduction Systems in "First Touch" and
Adhesion of Fungal Spores ................................... 1
1.2.1 First Touch or Initial Contact Triggers
the Infection Process ................................. 1
1.2.2 Adhesion or Close Contact Triggers Fungal Infection
Process ............................................... 3
1.2.3 Adhesion of Spores due to Hydrophobic Interaction ..... 3
1.2.4 Adhesion of Spores Is Accompanied by Release of
Extracellular Material ................................ 4
1.2.5 Involvement of Cutinases in Spore Adhesion ............ 5
1.2.6 Some Plant Signals May Be Needed for Adhesion of
Spores ................................................ 5
1.3 Signaling in Fungal Spore Germination ....................... 6
1.3.1 Plant Signals Trigger Structural Changes in Spores
before Germination .................................... 6
1.3.2 Plant-Surface Signals Trigger Spore Germination ....... 7
1.3.3 Flavonoids Signaling Spore Germination ................ 8
1.4 Signaling in Differentiation of Germ Tubes into Infection
Structures .................................................. 8
1.4.1 Adhesion of Germlings and Infection Structures ........ 8
1.4.2 Extracellular Matrix in Germling Adhesion ............. 9
1.4.3 Extracellular Matrix in Appressorial Adhesion ........ 11
1.4.4 Topographic Signals in Appressorium Formation ........ 11
1.4.5 Plant-Surface Wax Signals Appressorium Formation ..... 13
1.4.6 Cutin Monomers as Signal Molecules ................... 14
1.4.7 Ethylene Signals Appressorium Formation .............. 14
1.4.8 Fungal Signals in Induction of Appressorium
Formation ............................................ 15
1.5 Signal Transduction in Fungal Pathogenesis ................. 16
1.5.1 Transmembrane Receptor for Extracellular Signals ..... 16
1.5.2 G-Proteins ........................................... 17
1.5.3 Calcium/Calmodulin-Dependent Signaling ............... 20
1.5.4 cAMP/Protein Kinase Signaling Pathway ................ 21
1.5.5 Mitogen-Activated Protein Kinase Signaling
Cascades ............................................. 24
1.5.6 Lipid-Induced Protein Kinase Signaling ............... 28
1.5.7 РАК Signaling ........................................ 28
1.5.8 Phosphorylation and Dephosphorylation Cascades ....... 29
1.5.9 P-Type Adenosine Triphosphatase Signaling ............ 29
1.6 Genes Involved in Formation of Infection Structures ........ 30
1.7 Signals in Fungal Infection Process ........................ 32
1.7.1 Magnaporthe grisea ................................... 32
1.7.2 Blumeria graminis .................................... 34
1.7.3 Colletotrichum gloeosporioides ....................... 35
1.7.4 Ustilago maydis ...................................... 36
1.7.5 Fusarium oxysporum ................................... 37
1.8 Conclusion ................................................. 37
References ..................................................... 38
Chapter 2
Perception and Transduction of Pathogen Signals in Plants ...... 55
2.1 Introduction .............................................. 55
2.2 What Are Elicitors? ....................................... 56
2.3 Oligosaccharide Elicitors ................................. 57
2.3.1 Chitooligosaccharide Elicitors ...................... 57
2.3.2 Chitosan Elicitors .................................. 58
2.3.3 Oligoglucan Elicitors ............................... 58
2.3.4 Other Carbohydrate Elicitors ........................ 60
2.4 Protein/Peptide Elicitors ................................. 60
2.4.1 Elicitins ........................................... 60
2.4.2 Xylanase Elicitor ................................... 64
2.4.3 PaNie213 Elicitor .................................... 64
2.4.4 Nep1 Elicitor ....................................... 64
2.4.5 NIP1 Elicitor ....................................... 64
2.4.6 PB90 Elicitor ....................................... 65
2.5 Glycoprotein Elicitors .................................... 65
2.5.1 Carbohydrate Moiety in the Glycoprotein Elicitor
May Confer Elicitor Activity ........................ 65
2.5.2 Protein Moiety in Glycoprotein Elicitors May
Confer Elicitor Activity ............................ 66
2.5.3 Functions of Glycoprotein Elicitors ................. 67
2.6 Lipid Elicitors ........................................... 67
2.6.1 Sphingolipids ....................................... 67
2.6.2 Arachidonic and Eicosapentaenoic Acids .............. 68
2.6.3 Ergosterols ......................................... 68
2.7 Toxins as Elicitor Molecules .............................. 69
2.8 Plant Cell Wall-Degrading Enzymes as Elicitors ............ 69
2.9 Race-Specific and Cultivar-Specific Elicitors ............. 70
2.10 Specificity of General Elicitors .......................... 72
2.11 Endogenous Oligogalacturonide Elicitors ................... 73
2.12 Multiple Elicitors May Be Needed to Activate Defense
Responses ................................................. 74
2.12.1 Elicitor Complex .................................. 74
2.12.2 Network of Elicitor Molecules ..................... 74
2.13 Availability of Fungal Elicitors at the Site of Fungal
Invasion in Plants ........................................ 75
2.14 Receptors for Elicitor Signals in Plant Cell Membrane ..... 76
2.14.1 Receptor Sites for Binding Oligosaccharide
Elicitors ......................................... 76
2.14.2 Receptor Sites for Binding Proteinaceous
Elicitors ......................................... 77
2.14.3 Protein Kinases as Receptor Sites ................. 78
2.14.4 LRR-Type Receptors ................................ 78
2.14.5 Lectins as Receptors .............................. 79
2.14.6 Resistance Gene Products as Receptors ............. 79
2.15 Calcium Ion May Act as Second Messenger ................... 79
2.15.1 Function of Calcium Ion as Second Messenger ....... 79
2.15.2 Upstream Events of Ca2+ Signaling ................. 81
2.15.3 Downstream Events of Ca2+ Signaling ............... 82
2.16 Phosphorylation of Proteins as a Component in Signal
Transduction System ....................................... 83
2.16.1 Phosphorylation/Dephosphorylation Events .......... 83
2.16.2 Calcium Ion in Phosphorylation .................... 83
2.17 Mitogen-Activated Protein Kinase Cascades in Signal
Transduction .............................................. 84
2.18 Phospholipid-Signaling System ............................. 85
2.18.1 Plant Cell Membrane Phospholipids as Signal
Molecules ......................................... 85
2.18.2 Role of Phospholipase A in Phospholipid-
Signaling System .................................. 86
2.18.3 Phospholipase С in Phospholipid-Signaling
System ............................................ 87
2.18.4 Phospholipase D in Phospholipid-Signaling
System ............................................ 89
2.19 Anion Channels in Signal Transduction ..................... 90
2.19.1 Anion Channels in the Signaling System ............ 90
2.19.2 Upstream Events of Anion Channel-Signaling
System ............................................ 91
2.19.3 Downstream of Anion Channel-Signaling System ...... 91
2.20 Extracellular Alkahnization and Cytoplasmic
Acidification in Signaling System ......................... 91
2.21 Reactive Oxygen Species in Signal Transduction ............ 92
2.21.1 Oxidative Burst ................................... 92
2.21.2 Mechanisms of Production of Reactive Oxygen
Species ........................................... 93
2.21.2.1 Production of O2- ........................ 93
2.21.2.2 Production of H2O2 ....................... 94
2.21.2.3 Production of •OH Radical ................ 95
2.21.2.4 Production of Singlet Oxygen (1O2) ....... 95
2.21.3 Upstream of ROS Signaling ......................... 96
2.21.4 Downstream of ROS Signaling ....................... 96
2.22 Nitric Oxide in Signal Transduction ....................... 97
2.22.1 Increases in Nitric Oxide ......................... 97
2.22.2 Biosynthesis of Nitric Oxide ...................... 97
2.22.3 Upstream Events of Nitric Oxide Signaling ......... 98
2.22.4 Downstream Events of Nitric Oxide Signaling ....... 99
2.23 Salicylic Acid-Signaling System .......................... 100
2.23.1 Salicylic Acid in Signaling Defense Response in
Plants ........................................... 100
2.23.2 Biosynthesis of Salicylic Acid ................... 101
2.23.3 Signal Perception ................................ 102
2.23.4 Upstream Signals for Induction of Synthesis of
Salicylic Acid ................................... 102
2.23.5 Downstream of Salicylic Acid Signaling ........... 103
2.23.6 Methyl Salicylate ................................ 104
2.23.7 Salicylate-Independent Signaling Systems ......... 105
2.24 Jasmonate-Signaling Pathway .............................. 105
2.24.1 Jasmonate Signaling in Induction of Defense
Responses ........................................ 105
2.24.2 Biosynthesis of Jasmonates ....................... 106
2.24.3 Perception of Jasmonate Signals .................. 108
2.24.4 Jasmonate-Signaling System May Behave
Differently in Protecting Plants against
Various Pathogens ................................ 108
2.24.5 Induction of Intercellular and Interplant
Systemic Transduction of Jasmonate Signals ....... 109
2.24.6 Upstream of Jasmonate Signaling .................. 109
2.24.7 Downstream of Jasmonate Signaling ................ 109
2.24.8 Transcriptional Regulation of JA-Responsive
Genes ............................................ 109
2.24.9 Jasmonic Acid, Methyl Jasmonate, and Cyclic
Precursors and Derivatives of Jasmonic Acid as
Signal Molecules ................................. 110
2.25 Role of Systemin in Signal Transduction System ........... 111
2.26 Ethylene-Dependent Signaling Pathway ..................... 112
2.26.1 Ethylene-Signaling System Inducing Disease
Resistance or Susceptibility ..................... 112
2.26.2 Biosynthesis of Ethylene ......................... 112
2.26.3 Upstream Signals in Induction of Synthesis of
Ethylene ......................................... 113
2.26.4 Ethylene Signal Perception ....................... 114
2.26.5 Downstream Events in Ethylene Signaling .......... 114
2.27 Abscisic Acid Signaling .................................. 115
2.28 Fatty Acids as Systemic Signal Molecules ................. 116
2.29 Other Signaling Systems .................................. 116
2.30 Network and Interplay of Signaling Pathways .............. 116
2.30.1 Regulatory Interaction and Coordination among
Salicylate-, Jasmonate-, and Ethylene-Signaling
Pathways ......................................... 116
2.30.2 Coordinated Regulation of Ethylene- and
Jasmonate-Signaling Pathways ..................... 117
2.30.3 Interplay between Salicylate-and Jasmonate-
Signaling Pathways ............................... 118
2.30.4 Interplay between Salicylate and Ethylene
Pathways ......................................... 118
2.30.5 Cross Talk between Salicylate and Jasmonate/
Ethylene Pathways ................................ 119
2.30.6 Cross Talk between Abscisic Acid-, Jasmonate-,
and Ethylene-Dependent Signaling Pathways ........ 120
2.30.7 Regulatory Switches to Fine-Tune Signaling
Pathways ......................................... 121
2.31 Induction of Defense Genes May Require Different Signal
Transduction Systems ..................................... 121
2.32 Perception and Transduction of Pathogen Signals in
Plants Leading to Susceptibility ......................... 123
2.32.1 Differential Expression of Signaling System
Leading to Susceptibility or Resistance .......... 123
2.32.2 Slower Accumulation of Elicitor-Releasing
Enzymes in Susceptible Interactions .............. 124
2.32.3 Susceptible Varieties May Release Less Amount
of Elicitors from Fungal Pathogen Cell Walls ..... 124
2.32.4 Delayed Release of Elicitors in Susceptible
Interactions ..................................... 127
2.32.5 Elicitor of Compatible Pathogens Induces Less
Defense-Related Actions than That of
Incompatible Pathogens ........................... 127
2.32.6 Degradation of Fungal Elicitors by Plant
Enzymes in Plant Tissues May Lead to
Susceptibility ................................... 128
2.32.7 Fungal Pathogens May Degrade Host Elicitors
during Susceptible Interactions .................. 129
2.32.8 Elicitors May Be Released during Pathogenesis
but May Not Be Active or Less Active in
Susceptible Plants ............................... 130
2.32.9 Some Elicitors Do Not Act or Show Little
Activity on Susceptible Cultivars ................ 132
2.32.10 Speed of Expression of Signal Transduction
System May Determine Susceptibility or
Resistance ....................................... 134
2.32.11 Reduced Accumulation of Signals May Lead to
Susceptibility ................................... 134
2.32.12 Elicitors May Induce Genes Involved in
Suppression of Defense-Related Genes in
Susceptible Interactions ......................... 135
2.32.13 Suppressors Negating Elicitor-Induced Defense
Responses in Susceptible Interactions ............ 137
2.32.14 Susceptible Plants May Have Suppressors to
Suppress Action of Fungal Elicitors .............. 140
2.32.15 Downregulation of Functions of Elicitors in
Susceptible Interactions ......................... 140
2.32.16 Activation of an Unsuitable Signaling System
for Induction of Defense Responses May Lead to
Susceptibility ................................... 141
2.33 Signaling Systems in Susceptible Interactions ............ 143
2.33.1 Abscisic Acid-Signaling System ................... 143
2.33.2 Ethylene-Signaling System ........................ 144
2.33.3 Signal Transduction Systems May Induce
Susceptibility-Related Responses ................. 144
2.34 Conclusion ............................................... 144
References .................................................... 147
Chapter 3
Disease Resistance and Susceptibility Genes in Signal
Perception and Emission ....................................... 193
3.1 Introduction ............................................. 193
3.2 Molecular Structure of Resistance Genes .................. 195
3.2.1 LRR Domains ........................................ 195
3.2.2 NBS Domains ........................................ 195
3.3 Classification of Resistance Genes Based on Molecular
Structure of R Gene-Encoded Proteins ..................... 196
3.3.1 Resistance Genes Encoding TIR-NBS-LRR Proteins ..... 196
3.3.2 Resistance Genes Encoding Non-TIR-NBS-LRR
Proteins ........................................... 197
3.3.3 Resistance Genes Encoding LRR Proteins Lacking
NBS Domain ......................................... 199
3.3.4 Resistance Genes Encoding Proteins Lacking LRR
Domain ............................................. 200
3.3.4.1 LRD Proteins ............................... 200
3.3.4.2 Intracellular Protein Kinases .............. 200
3.3.4.3 Transmembrane Proteins ..................... 201
3.3.4.4 Lectin-Туре Proteins ....................... 202
3.3.4.5 Heat Shock Protein-Like Proteins ........... 202
3.3.4.6 NADPH-Dependent Reductase-Туре Protein ..... 202
3.3.4.7 Plant eR Genes Encoding Photorespiratory
Peroxisomal Enzyme Proteins ................ 202
3.4 Molecular Structure of Recessive Genes ................... 202
3.4.1 Barley mlo Gene .................................... 202
3.4.2 Arabidopsis PMR6 Gene .............................. 203
3.4.3 Arabidopsis RRS1-R Gene ............................ 203
3.4.4 Arabidopsis ssi4 Gene .............................. 203
3.5 Perception of Pathogen Signals by Resistance Genes ....... 204
3.5.1 Functions of Different Domains of R Proteins in
Pathogen Recognition ............................... 204
3.5.1.1 LRR Domain ................................ 204
3.5.1.2 NBS Domain ................................ 204
3.5.1.3 TIR Domain ................................ 205
3.5.1.4 CC Domain ................................. 205
3.5.1.5 C-Terminal Non-LRR Region ................. 206
3.5.1.6 C-Terminus Transcriptional Activation
Domain .................................... 206
3.5.1.7 Protein Kinase Domain ..................... 206
3.5.1.8 Transmembrane Domain ...................... 206
3.5.1.9 Calmodulin-Binding Protein ................ 207
3.5.1.10 Lectin-Туре Protein ....................... 207
3.5.1.11 Heat Shock Protein (HSP)-Like Protein ..... 207
3.5.2 R Gene Product May Act as a Receptor That
Recognizes an AVR Gene Product ..................... 207
3.5.3 R Protein May Detect Binding of an AVR Protein to
a Different Protein in the Plant ................... 208
3.6 Activation of R Protein and Emission of Signals to
Other Components in the Cell ............................. 209
3.7 Downstream Components of R Gene-Signaling Systems ........ 211
3.7.1 Regulatory Genes (or Complementary Genes or R
Gene-Signaling Components) ......................... 211
3.7.2 EDS1-PAD4 Proteins ................................. 212
3.7.3 NDR1 Proteins ...................................... 213
3.7.4 RAR1-SGT1-HSP90 Proteins ........................... 214
3.7.4.1 RAR1 ....................................... 214
3.7.4.2 SGT1 ....................................... 215
3.7.4.3 RAR1/SGT1 Complex .......................... 217
3.7.4.4 Interaction of RAR1/SGT1 with HSP90 ........ 217
3.7.5 NDR1 ............................................... 218
3.7.6 Prf-Pto-Pti Signaling System ....................... 219
3.7.7 Other Regulatory Genes ............................. 219
3.8 Downstream Signaling Events in R Gene-Mediated
Resistance ............................................... 221
3.9 Susceptibility Genes in Signal Transduction .............. 222
3.9.1 Susceptibility Alleles of Resistance Genes ......... 222
3.9.2 Susceptibility Genes .............................. 222
3.9.3 Resistance Gene May Act as Susceptibility Gene
against Some Pathogens ............................. 223
3.9.4 Low Expression of Resistance Genes May Lead to
Susceptibility ..................................... 224
3.9.5 Susceptibility Alleles of Resistance Genes May
Negate the Function of Resistance Genes ............ 224
3.9.6 Suppressor Genes ................................... 225
3.10 Conclusion ............................................... 225
References .................................................... 227
Chapter 4
Cell Death Programs during Fungal Pathogenesis ................ 243
4.1 Introduction ............................................. 243
4.2 Cell Death in Resistant Interactions ..................... 243
4.2.1 Programmed Cell Death .............................. 243
4.2.2 Hypersensitive Cell Death .......................... 244
4.2.3 Spontaneous Cell Death ............................. 244
4.2.4 Runaway Cell Death ................................. 245
4.2.5 Cell Death-Inducing Systemic Acquired Resistance ... 245
4.3 Molecular Mechanism of Induction of Hypersensitive Cell
Death .................................................... 245
4.3.1 Mediators, Regulators, and Executioners of Cell
Death .............................................. 245
4.3.2 R Gene Signals Involved in Triggering Cell Death ... 246
4.3.3 Reactive Oxygen Species in Cell Death .............. 246
4.3.4 Nitric Oxide in Cell Death ......................... 249
4.3.5 Bax Family of Proteins ............................. 250
4.3.6 Ion-Conducting Channels ............................ 251
4.3.7 Function of Mitochondrion in Induction of Cell
Death .............................................. 251
4.3.8 Proteolytic Enzymes ................................ 251
4.3.8.1 Plant Caspases ............................. 251
4.3.8.2 Vacuolar Processing Enzymes (VPEs) ......... 252
4.3.8.3 Metacaspases ............................... 252
4.3.8.4 Other Types of Proteolytic Enzymes ......... 253
4.3.9 Probable Sequence in Induction of Hypersensitive
Cell Death ......................................... 253
4.4 Molecular Mechanism of Induction of Spontaneous Cell
Death .................................................... 253
4.4.1 Spontaneous Cell Death-Regulating Genes ............ 253
4.4.2 Salicylic Acid ..................................... 255
4.4.3 Ethylene ........................................... 255
4.4.4 Phosphatidic Acid .................................. 255
4.5 Molecular Mechanism of Induction of Runaway Cell Death ... 256
4.6 Role of Cell Death in Induction of Systemic Acquired
Resistance ............................................... 257
4.7 Susceptibility-Related Cell Death ........................ 258
4.8 Molecular Mechanisms in Induction of Cell Death in
Susceptible Interactions ................................. 258
4.8.1 Mediators, Regulators, and Executioners of
Susceptibility-Related Plant Cell Death ............ 258
4.8.2 Reactive Oxygen Species ............................ 259
4.8.3 Proteolytic Enzymes ................................ 259
4.8.4 Calcium Ion ........................................ 260
4.8.5 Salicylate, Ethylene, and Jasmonate ................ 260
4.8.6 Sphingolipid Metabolism ............................ 262
4.8.7 Extracellular ATP Levels ........................... 262
4.9 What Is the Function of Cell Death in Fungal
Pathogenesis? ............................................ 262
4.10 Conclusion ............................................... 264
References .................................................... 264
Chapter 5
Cell Wall Degradation and Fortification ....................... 275
5.1 Introduction ............................................. 275
5.2 Structure of Cuticle ..................................... 275
5.3 Penetration of Epicuticular Waxy Layer by Pathogens ...... 276
5.4 Production of Cutinases to Breach Cuticle Barrier ........ 276
5.5 Genes Encoding Cutinases ................................. 277
5.6 Plant Signals Triggering Fungal Cutinases ................ 278
5.7 Importance of Cutinases in Penetration of Cuticle ........ 279
5.8 Cutinases as Virulence/Pathogenicity Factors ............. 280
5.9 Melanins in Fungal Penetration of Cuticle Barrier ........ 281
5.9.1 Biosynthesis of Melanins .......................... 281
5.9.2 Melanins Aid in Penetration of Cuticle Barrier
by Fungal Pathogens ............................... 283
5.10 Degradation of Pectic Polysaccharides .................... 285
5.10.1 Types of Pectic Polysaccharides ................... 285
5.10.2 Types of Pectic Enzymes ........................... 285
5.10.3 Fungal Pathogens Produce Multiple Pectic
Enzymes ........................................... 286
5.10.4 Genes Encoding Pectic Enzymes ..................... 287
5.10.5 Evidences to Show That Pectic Enzymes Aid
Pathogens to Penetrate Cell Wall .................. 288
5.10.5.1 Immunocytochemical Evidences ............. 288
5.10.5.2 Evidences by Showing Protection of
the Host by Inhibition of Pectic
Enzymes with Specific Antibodies ......... 289
5.10.5.3 Evidences Showing Protection of Host
Plants by Inhibition of Pectic Enzymes
with Selective Inhibitors ................ 290
5.10.5.4 Evidences Using Pectic Enzyme-Deficient
Fungal Isolates .......................... 290
5.10.5.5 Evidences Showing Correlation between
the Level of Pectic Enzymes and
Virulence ................................ 291
5.10.5.6 Evidences Showing Enhancement of
Virulence by Gene Transfer ............... 291
5.10.5.7 Evidences Showing Decrease in Virulence
by Gene Disruption ....................... 291
5.10.6 Plant Signals to Induce Pectic Enzymes ............ 291
5.10.7 Host Cell Wall Differs in Its Susceptibility to
Pectic Enzymes .................................... 292
5.10.8 Cell Wall Proteins Modulate Pectic Enzyme
Activity .......................................... 292
5.11 Pathogens Produce Cellulolytic Enzymes to Breach Cell
Wall Barrier ............................................. 294
5.12 Fungal Hemicellulases in Plant Cell Wall Degradation ..... 295
5.13 Degradation of Cell Wall Structural Proteins ............. 296
5.14 Requirement of Several Cell Wall-Degrading Enzymes to
Degrade the Complex-Natured Cell Wall .................... 297
5.15 Production of Suitable Enzymes in Appropriate Sequence
by Fungal Pathogens ...................................... 297
5.16 Reinforcement of Host Cell Wall during Fungal Invasion ... 298
5.17 Papillae Suppress Fungal Penetration ..................... 298
5.18 Callose Deposition in Cell Wall .......................... 300
5.19 How Do Pathogens Overcome the Papillae and Callose
Barriers? ................................................ 301
5.19.1 Pathogen Delays Papillae Formation ............... 301
5.19.2 Pathogens May Suppress Callose Synthesis in
Susceptible Interactions ......................... 302
5.19.3 Pathogens May Be Able to Penetrate the Papillae
Barrier .......................................... 303
5.19.4 Pathogens May Degrade Callose by Producing
β-1,3-Glucanase .................................. 303
5.20 Accumulation of Hydroxyproline-Rich Glycoproteins in
Plant Cell Walls ......................................... 304
5.20.1 Host Cell Wall Responds to Fungal Invasion by
Accumulating HRGP ................................ 304
5.20.2 Signals Triggering Accumulation of HRGPs ......... 304
5.20.3 Host Cell Wall Responds to Fungal Invasion by
Strengthening Its HRGPs by Glycosylation ......... 305
5.20.4 Insolubilization of HRGPs in Host Cell Wall ...... 305
5.20.5 Enrichment of HRGPs by Lignin Deposition ......... 305
5.20.6 Some HRGPs May Immobilize Plant Pathogens ........ 306
5.20.7 How Does Pathogen Overcome HRGP Barrier? ......... 306
5.20.7.1 Less Accumulation of HRGPs in
Compatible Interactions ................. 306
5.20.7.2 Pathogen Overcomes HRGP Barrier by
Delaying Accumulation of HRGPs in Host
Cell Wall ............................... 306
5.21 Cell Wall-Bound Phenolics and Lignins .................... 307
5.21.1 Fortification of Plant Cell Wall by Phenolics
and Lignin ........................................ 307
5.21.2 Biosynthesis of Phenolics and Lignins ............. 308
5.21.3 Phenolic Deposition in Host CeII Wall in
Response to Fungal Invasion ....................... 308
5.21.4 Host Cell Wall Responds to Fungal Invasion by
Activating Enzymes Involved in Synthesis of
Wall-Bound Phenolics .............................. 310
5.21.5 How Does the Pathogen Overcome the Cell
Wall-Bound Phenolics to Cause Disease? ............ 311
5.21.5.1 Pathogen Suppresses Accumulation of
Phenolics in Host Cell Wall .............. 311
5.21.5.2 Pathogen Delays Synthesis of Cell
Wall-Bound Phenolics ..................... 312
5.21.6 Lignification during Fungal Pathogenesis .......... 312
5.21.6.1 Host Cell Wall Responds to Fungal
Invasion by Increasing Lignification
Process .................................. 312
5.21.6.2 Pathogen Suppresses Lignin Deposition .... 313
5.21.6.3 Pathogen Suppresses Enzymes Involved in
Lignin Biosynthesis ...................... 314
5.21.6.4 How Does Pathogen Suppress
Lignification in Host Cell Wall? ......... 315
5.22 Suberization during Fungal Pathogenesis .................. 316
5.22.1 Host Cell Wall Responds to Fungal Invasion by
Suberization ...................................... 316
5.22.2 Biosynthesis of Suberin in Pathogen-Inoculated
Host Cell Wall .................................... 316
5.22.3 Pathogen Delays Suberin Accumulation .............. 317
5.22.4 Pathogen May Suppress Suberin-Synthesizing
Enzymes ........................................... 317
5.22.5 Pathogens May Penetrate the Suberized Walls of
Host Cells ........................................ 318
5.23 Deposition of Mineral Elements in Host Cell Wall in
Response to Fungal Invasion .............................. 318
5.23.1 Silicon Deposition ................................ 318
5.23.2 Calcium Deposition in Papillae .................... 318
5.23.3 Manganese Accumulation in Papillae ................ 319
5.24 Conclusion ............................................... 319
References .................................................... 320
Chapter 6
Induction and Evasion of Pathogenesis-Related Proteins ........ 345
6.1 Introduction ............................................. 345
6.2 Multiplicity of PR Proteins .............................. 346
6.3 Classification of PR Proteins ............................ 347
6.3.1 PR-1 Proteins ..................................... 347
6.3.2 PR-2 Proteins ..................................... 348
6.3.3 PR-3 Proteins ..................................... 349
6.3.4 PR-4 Proteins ..................................... 350
6.3.5 PR-5 Proteins ..................................... 351
6.3.6 PR-6 Proteins ..................................... 351
6.3.7 PR-7 Proteins ..................................... 352
6.3.8 PR-8 Proteins ..................................... 352
6.3.9 PR-9 Proteins ..................................... 352
6.3.10 PR-10 Proteins .................................... 353
6.3.11 PR-11 Proteins .................................... 353
6.3.12 PR-12 Proteins .................................... 353
6.3.13 PR-13 Proteins .................................... 354
6.3.14 PR-14 Proteins .................................... 354
6.3.15 PR-15 Proteins .................................... 354
6.3.16 PR-16 Proteins .................................... 355
6.3.17 PR-17 Proteins .................................... 355
6.3.18 Chitosanases ...................................... 355
6.4 Induction of PR Proteins during Fungal Pathogenesis ...... 355
6.5 Genes Encoding PR Proteins ............................... 356
6.6 Transcription of PR Genes ................................ 357
6.7 Signals Involved in Transcriptional Induction of PR
Genes .................................................... 358
6.7.1 Induction of PR Genes by Elicitors ................ 358
6.7.2 Induction of PR Genes by Salicylic Acid ........... 359
6.7.3 Induction of PR Genes by Ethylene ................. 360
6.7.4 Induction of PR Genes by Jasmonic Acid/
Jasmonate ......................................... 362
6.7.5 Induction of PR Proteins May Require Different
Signal Transduction Systems ....................... 363
6.7.6 Synergistic Effect of Different Signals ........... 364
6.7.7 Antagonistic Effect of Different Signals .......... 364
6.8 PR Proteins Are Synthesized as Larger Precursors ......... 364
6.9 Secretion of PR Proteins ................................. 365
6.9.1 Secretory Pathways ................................ 365
6.9.2 Site of Accumulation of PR Proteins ............... 366
6.10 PR Proteins May Be Involved in Inhibition of Pathogen
Development .............................................. 367
6.10.1 Inhibition of Fungal Growth by PR Proteins In
Vitro ............................................. 367
6.10.2 Inhibition of Fungal Growth by PR Proteins In
Vivo .............................................. 369
6.10.3 Some PR Proteins May Be Involved in Release of
Elicitor Molecules in Planta ...................... 370
6.10.4 Some PR Proteins May Be Involved in
Reinforcement of Cell Wall Structures ............. 370
6.11 PR Proteins May Be Involved in Triggering Disease
Resistance ............................................... 370
6.11.1 Demonstration of the Role of PR Proteins in
Disease Resistance Using Chemical or Biological
Elicitors ......................................... 370
6.11.2 Demonstration of Role of PR Proteins in Disease
Resistance by Inducing Mutation ................... 371
6.11.3 Demonstration of Role of PR Proteins in Disease
Resistance by Developing Transgenic Plants ........ 371
6.11.4 Demonstration of the Role of PR Proteins by
Developing Transgenic Plants with Antisense
Suppression of PR Genes ........................... 373
6.12 How Do Pathogens Overcome Fungitoxic PR Proteins of
the Host? ................................................ 373
6.12.1 Slower Accumulation of PR Proteins May Enable
Pathogens to Escape the Antifungal Action of PR
Proteins .......................................... 373
6.12.2 Pathogens May Shed Away from Their Cell Wall
the Substrate for the PR Proteins of Enzymatic
Nature and Avoid Their Lytic Enzyme Action ........ 379
6.12.3 Pathogens May Produce Enzymes That Protect Them
from Fungitoxic Action of PR-3 Proteins ........... 380
6.12.4 Pathogens May Produce Enzymes to Inhibit
Activity of Some PR Proteins ...................... 381
6.12.5 Less Elicitor Is Released from Pathogen's Cell
Wall to Activate Synthesis of PR Proteins ......... 381
6.12.6 PR Proteins Are Degraded Quickly in
the Susceptible Host Tissues ...................... 382
6.12.7 Site of Accumulation of Some PR Proteins May
Determine Susceptibility or Resistance ............ 382
6.12.8 Adaptation of Pathogens to PR Proteins ............ 384
6.12.9 Some PR Proteins May Not Be Involved in Disease
Resistance ........................................ 385
6.13 Conclusion ............................................... 385
References .................................................... 386
Chapter 7
Evasion and Detoxification of Secondary Metabolites ........... 411
7.1 Introduction ............................................. 411
7.2 Chemical Structural Classes of Phytoalexins .............. 412
7.3 Biosynthesis of Isoflavonoid Phytoalexins ................ 414
7.3.1 Phaseollin and Related Compounds ................... 414
7.3.2 Glyceollins ........................................ 418
7.3.3 Medicarpin ......................................... 420
7.3.4 Pisatin ............................................ 423
7.4 Biosynthesis of Flavanone Phytoalexins ................... 424
7.5 Biosynthesis of Coumarin Phytoalexins .................... 424
7.6 Biosynthesis of Stilbene Phytoalexins .................... 426
7.7 Biosynthesis of Terpenoid Phytoalexins ................... 426
7.8 Biosynthesis of Indole-Based Sulfur-Containing
Phytoalexins ............................................. 430
7.9 Biosynthesis of Alkaloid Phytoalexins .................... 431
7.10 Site of Synthesis of Phytoalexins ........................ 432
7.11 Phytoalexins Are Fungitoxic .............................. 432
7.12 How Do Pathogens Overcome the Antifungal Phytoalexins? ... 433
7.12.1 Pathogens May Detoxify Phytoalexins ............... 433
7.12.2 Induction of Phytoalexins May Be Delayed in
Susceptible Interactions .......................... 436
7.12.3 Pathogen May Suppress Accumulation of
Phytoalexins in Susceptible Hosts ................. 438
7.12.4 Amount of Accumulation of Phytoalexins May Be
Less in Susceptible Interactions Compared with
Resistant Interactions ............................ 439
7.12.5 Highly Toxic Phytoalexins May Not Accumulate in
Susceptible Interactions .......................... 439
7.12.6 Some Phytoalexins May Not Be Produced in
Susceptible Interactions .......................... 439
7.12.7 Some Phytoalexins May Not Have Any Role in
Defense Mechanisms of Plants ...................... 440
7.13 Chemical Structural Classes of Phytoanticipins ........... 440
7.14 Phenolics as Phytoanticipins ............................. 440
7.15 Toxicity of Phenolics to Pathogens ....................... 441
7.16 How Does Pathogen Overcome the Antifungal Phenolics? ..... 441
7.16.1 Pathogen May Degrade Phenolics to Nontoxic
Products .......................................... 441
7.16.2 Pathogen May Suppress Increased Synthesis of
Phenolics in Plants ............................... 443
7.16.3 Pathogen May Suppress Phenol Biosynthetic
Enzymes ........................................... 443
7.16.4 Pathogen May Suppress Phenolic Metabolism by Its
Suppressor Molecule ............................... 443
7.16.5 Pathogen May Suppress Phenolic Metabolism by
Producing Toxins .................................. 443
7.16.6 Pathogen May Suppress Oxidation of Phenolics by
Inhibiting Polyphenol Oxidase ..................... 444
7.16.7 Phenolics Are Fungitoxic but They May Not
Accumulate to Fungitoxic Level during
Pathogenesis in Some Plant-Pathogen
Interactions ...................................... 444
7.17 Saponins as Phytoanticipins .............................. 445
7.18 Glucosinolates as Phytoanticipins ........................ 447
7.18.1 Biosynthesis of Glucosinolates .................... 447
7.18.2 Toxicity of Glucosinolates to Fungal Pathogens .... 448
7.18.3 How Does the Pathogen Overcome Toxicity of
Glucosinolates? ................................... 448
7.18.3.1 Concentration of Glucosmolates May Be
Less in Susceptible Tissues .............. 448
7.18.3.2 Glucosinolates May Not Be Involved in
Disease Resistance Unless the Tissue Is
Damaged .................................. 448
7.19 Cyanogenic Glucosides .................................... 450
7.20 Dienes ................................................... 450
7.21 Conclusion ............................................... 450
References .................................................... 451
Chapter 8
Toxins in Disease Symptom Development ......................... 469
8.1 Introduction .............................................. 469
8.2 Importance of Toxins in Disease Development ............... 471
8.3 Toxins Suppress Host-Defense Mechanisms ................... 472
8.4 Toxins Cause Cell Membrane Dysfunction .................... 473
8.4.1 Permeability Changes ................................ 473
8.4.2 Changes in Membrane-Bound ATPases ................... 474
8.4.2.1 H+-ATPase Is Stimulated ..................... 474
8.4.2.2 H+-ATPase Is Inhibited ...................... 477
8.4.3 Inhibition of Calmodulin Activity ................... 477
8.4.4 Alteration in Membrane Potential .................... 477
8.4.5 Toxins Form Ion Channels in Plant Cell
Membranes ........................................... 479
8.4.6 Modification of Membrane Phospholipids .............. 479
8.4.7 Toxin-Induced Active Oxygen Species Induce
Membrane Dysfunction ................................ 480
8.4.8 Mitochondrial Membrane Dysfunction .................. 481
8.5 How Do Pathogens Induce Membrane Dysfunction Only in
Susceptible Hosts? ........................................ 483
8.5.1 Detoxification of Phytotoxins, Which Occurs in
Resistant Hosts, Does Not Occur in Susceptible
Hosts ............................................... 483
8.5.2 Susceptible Tissues May Have Toxin Receptors
Which May Be Absent in Resistant Tissues ............ 484
8.5.3 Susceptible Tissues May Be More Sensitive to
Toxins .............................................. 486
8.5.4 Specific Protein Synthesized after Toxin
Exposure May Confer Host Specificity ................ 487
8.5.5 Proteins of Susceptible Hosts May Enhance
Potential of Pathogens to Produce Toxins ............ 487
8.5.6 Sucrose Influx May Have Correlation with
Sensitivity to Toxin ................................ 487
8.5.7 Transport of Toxin to Cytoplasm May Occur Only
in Susceptible Interactions ......................... 488
8.6 Conclusion ................................................ 488
References .................................................... 489
Index ......................................................... 499
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